Rui Zhang1, You-Heng Wei2, Chun-Yan Zhao1, Hong-Yuan Song1, Ni Shen1, Xiao Cui1, Xin Gao1, Zhong-Tian Qi3, Ming Zhong1, Wei Shen1. 1. Department of Ophthalmology, Changhai Hospital, Second Military Medical University, Shanghai 200433, China. 2. State Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Sciences, Fudan University, Shanghai 200438, China. 3. Department of Microbiology, Second Military Medical University, Shanghai 200433, China.
Abstract
AIM: To study the effect of discoidin I-like domaincontaining protein 3 (EDIL3) depletion on the proliferation and epithelial-mesenchymal transition (EMT) in human lens epithelial cells (LECs). METHODS: RNA interference was used to inhibit the expression of EDIL3 in human LECs in vitro. The morphology of cells was observed using an inverted microscope. Cell proliferation was assessed using EdU kit. Cell migration was investigated using Transwell chamber and EMT of LECs was assessed using confocal microscope and Western blotting. The transforming growth factor β (TGFβ) pathway was investigated using Western blotting. RESULTS: The data showed that silencing EDIL3 expression changed LECs morphology and suppressed LECs proliferation (P<0.05) and migration (P<0.01). Furthermore, the result of Western blotting showed that EDIL3 depletion reduced the expression of α-smooth muscle actin (α-SMA) (P<0.001) and vimentin (P<0.01), while increased the expression of E-cadherin (P<0.001). EDIL3 depletion could suppress the phosphorylation of Smad2 (P<0.01) and Smad3 (P<0.01) and the activation of exracellular signal regulated kinase (ERK) (P<0.05). CONCLUSION: The findings indicate that EDIL3 might participate in the proliferation and EMT in LECs via TGFβ pathway and may be a potential therapeutic target for the treatment of posterior capsule opacification.
AIM: To study the effect of discoidin I-like domaincontaining protein 3 (EDIL3) depletion on the proliferation and epithelial-mesenchymal transition (EMT) in human lens epithelial cells (LECs). METHODS: RNA interference was used to inhibit the expression of EDIL3 in human LECs in vitro. The morphology of cells was observed using an inverted microscope. Cell proliferation was assessed using EdU kit. Cell migration was investigated using Transwell chamber and EMT of LECs was assessed using confocal microscope and Western blotting. The transforming growth factor β (TGFβ) pathway was investigated using Western blotting. RESULTS: The data showed that silencing EDIL3 expression changed LECs morphology and suppressed LECs proliferation (P<0.05) and migration (P<0.01). Furthermore, the result of Western blotting showed that EDIL3 depletion reduced the expression of α-smooth muscle actin (α-SMA) (P<0.001) and vimentin (P<0.01), while increased the expression of E-cadherin (P<0.001). EDIL3 depletion could suppress the phosphorylation of Smad2 (P<0.01) and Smad3 (P<0.01) and the activation of exracellular signal regulated kinase (ERK) (P<0.05). CONCLUSION: The findings indicate that EDIL3 might participate in the proliferation and EMT in LECs via TGFβ pathway and may be a potential therapeutic target for the treatment of posterior capsule opacification.
Entities:
Keywords:
discoidin I-like domain-containing protein 3; epithelial-mesenchymal transition; human lens epithelial cells; transforming growth factor β
Authors: Lisanne M Nibourg; Edith Gelens; Roel Kuijer; Johanna M M Hooymans; Theo G van Kooten; Steven A Koopmans Journal: Exp Eye Res Date: 2015-03-14 Impact factor: 3.467
Authors: Thomas Sauvigny; Malik Alawi; Linda Krause; Sina Renner; Michael Spohn; Alice Busch; Verena Kolbe; Janine Altmüller; Britt-Sabina Löscher; Andre Franke; Christian Brockmann; Wolfgang Lieb; Manfred Westphal; Nils Ole Schmidt; Jan Regelsberger; Georg Rosenberger Journal: J Neurol Date: 2020-05-04 Impact factor: 4.849